These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Myocardial characteristics of pressure overload hypertrophy. A structural and functional study.
    Author: Breisch EA, White FC, Bloor CM.
    Journal: Lab Invest; 1984 Sep; 51(3):333-42. PubMed ID: 6236333.
    Abstract:
    The effects of pressure overload hypertrophy were studied in the left ventricular myocardium of young adult cats. Hypertrophy was induced by a 90% constriction of the ascending aorta, and animals were studied 4, 7, 30, 120, and 248 days after constriction. Cardiac hypertrophy, as determined by heart weight, was evident at each experimental time period. Ultrastructural data indicate that during the early stages of hypertrophy (4 and 7 days) there is an enhancement of the myofibrillar volume relative to the mitochondrial volume. After 30 days the normal balance between the myofibrillar and mitochondrial volumes has been reestablished. The later stages of hypertrophy (120 and 248 days) are characterized by a reduced mitochondrial volume relative to the myofibrillar volume. This late stage of hypertrophy (248 days) is also characterized by reduced surface densities of the T-tubular and diadic junctional systems. Analysis of the microvasculature indicated that capillary density decreased with increasing time of hypertrophy. The effects of chronic hypertrophy on myocardial blood flow were also measured. In hypertrophied hearts, coronary reserve, measured as the percentage increase in blood flow from control to near maximal flow during adenosine infusion, was reduced. Left ventricular minimal coronary resistance (per gram) was elevated during hypertrophy. These results indicate that the alterations in flow reserve are largely due to the reduced capillary density. This, combined with the inability of the myocardium at the cellular level to maintain normal structural parameters, may play an important role in the transition of a compensated heart to a failing heart.
    [Abstract] [Full Text] [Related] [New Search]